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Hemangioma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jesus Rosario Hernandez, M.D. [2] Nawal Muazam M.D.[3]Amandeep Singh M.D.[4]

Synonyms and keywords: Haemangioma

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Hemangioma was first described by Dr. Robert Liston, a British surgeon, in 1843.[1] Hemangioma may be classified according to International Society for the Study of Vascular Anomalies into six subtypes: Infantile hemangioma, congenital hemangioma, tufted angioma, spindle-cell hemangioma, epithelioid hemangioma, and lobular capillary hemangioma.[2][3] Development of hemangioma is the result of genetic mutations, overexpression of angiogenic fators and downregulation of inhibitors of angiogenesis.[4] Hemangioma may be associated with POEMS syndrome and Castleman disease. On gross pathology, spongy with vascular compartments of various sizes separated by fibrous tissue are findings of hemangioma.[4] On microscopic histopathological analysis, channels lined by benign endothelium containing red blood cells are findings of hemangioma.[5] There are no established causes for hemangioma.[6] Hemangioma must be differentiated from other diseases such as: Congenital hemangioma, kaposiform hemangioendothelioma, tufted angioma, and nevus flammeus, and pyogenic granuloma.[7] The prevalence of infantile hemangioma is estimated to be up to 10% in general population.[3] Hemangioma commonly affects infants.[6] Females are more commonly affected with hemangioma than males.[6] Common risk factors in the development of hemangioma are female gender, prematurity, low birth weight, and fair skin.[3] According to the United States Preventive Services Task Force, there is insufficient evidence to recommend routine screening for hemangioma.[8] If left untreated, 20% of patients with hemangioma may progress to develop ulceration, hemorrhage, infection, and high output cardiac failure.[9] Common complications of hemangioma include ischemia, necrosis, ulceration, and bleeding.[3] Prognosis is generally good. Physical examination findings of superficial hemangioma include well-demarcated, flat, and erythematous red patches.[3] The majority of cases of hemangioma are self-limited. Patients with small, stable hemangiomas in non-vital sites are treated with “wait and see” approach, whereas patients with fast growth of hemangioma are treated medically.[6] Surgery is not the first-line treatment option for patients with hemangioma. It is usually reserved for patients with either massive protuberant proliferating hemangioma and lesions that are refractory to less invasive treatments.[7][3]

Historical Perspective

Hemangioma was first described by Dr. Robert Liston, a British surgeon, in 1843.[1]

Classification

Hemangioma may be classified according to International Society for the Study of Vascular Anomalies into six subtypes: Infantile hemangioma, congenital hemangioma, tufted angioma, spindle-cell hemangioma, epithelioid hemangioma, and lobular capillary hemangioma.[2][3]

Pathophysiology

Development of hemangioma is the result of genetic mutations, overexpression of angiogenic fators and downregulation of inhibitors of angiogenesis.[4] Hemangioma may be associated with POEMS syndrome and Castleman disease. On gross pathology, spongy with vascular compartments of various sizes separated by fibrous tissue are findings of hemangioma.[4] On microscopic histopathological analysis, channels lined by benign endothelium containing red blood cells are findings of hemangioma.[5]

Causes

There are no established causes for hemangioma.[6]

Differentiating Hemangioma from other Diseases

Hemangioma must be differentiated from other diseases such as: Congenital hemangioma, kaposiform hemangioendothelioma, tufted angioma, and nevus flammeus, and pyogenic granuloma.[7]

Epidemiology and Demographics

The prevalence of infantile hemangioma is estimated to be up to 10% in general population.[3] Hemangioma commonly affects infants.[6] Females are more commonly affected with hemangioma than males.[6]

Risk Factors

Common risk factors in the development of hemangioma are female gender, prematurity, low birth weight, and fair skin.[3]

Screening

According to the United States Preventive Services Task Force, there is insufficient evidence to recommend routine screening for hemangioma.[8]

Natural History, Complications and Prognosis

If left untreated, 20% of patients with hemangioma may progress to develop ulceration, hemorrhage, infection, and high output cardiac failure.[9] Common complications of hemangioma include ischemia, necrosis, ulceration, and bleeding.[3] Prognosis is generally good.

Diagnosis

Staging

There is no established system for the staging of hemangioma.

History and symptoms

Symptoms of hemangioma include: flat, and erythematous red patches.[3]

Physical Examination

Physical examination findings of superficial hemangioma include well-demarcated, flat, and erythematous red patches.[3]

Laboratory Findings

There are no diagnostic lab findings associated with hemangioma.

CT

On CT scan, hemangioma of the liver is characterized by dynamic enhancement pattern related to the size of its vascular space.[2]

MRI

Ultrasound

Ultrasound may be helpful in the diagnosis of hemangioma. Findings on ultrasound suggestive of hemangioma include fat, phleboliths or prominent vascular channels.[10]

Treatment

Medical therapy

The majority of cases of hemangioma are self-limited. Patients with small, stable hemangiomas in non-vital sites are treated with “wait and see” approach, whereas patients with fast growth of hemangioma are treated medically.[6]

Surgery

Surgery is not the first-line treatment option for patients with hemangioma. It is usually reserved for patients with either massive protuberant proliferating hemangioma and lesions that are refractory to less invasive treatments.[7][3]

Primary Prevention

There are no primary or secondary preventive measures available for hemangioma.

References

  1. ↑ 1.0 1.1 Liston R. Case of erectile tumour in the popliteal space.-Removal. Med Chir Trans. 1843;26:120-32.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2116921/pdf/medcht00056-0152.pdf
  2. ↑ 2.0 2.1 2.2 Hemangioma. Dr Tim Luijkx and Dr Donna D’Souza et al. Radiopaedia (2015). http://radiopaedia.org/articles/haemangioma. Accessed on November 12, 2015
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 Richter, Gresham T.; Friedman, Adva B. (2012). “Hemangiomas and Vascular Malformations: Current Theory and Management”. International Journal of Pediatrics. 2012: 1–10. doi:10.1155/2012/645678. ISSN 1687-9740.
  4. ↑ 4.0 4.1 4.2 4.3 Papafragkakis, Haris; Moehlen, Martin; Garcia-Buitrago, Monica T.; Madrazo, Beatrice; Island, Eddie; Martin, Paul (2011). “A Case of a Ruptured Sclerosing Liver Hemangioma”. International Journal of Hepatology. 2011: 1–5. doi:10.4061/2011/942360. ISSN 2090-3456.
  5. ↑ 5.0 5.1 Microscopic features of hemangioma. Librepathology (2015). http://librepathology.org/wiki/index.php/Hemangioma. Accessed on November 12, 2015
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 Zheng JW, Zhang L, Zhou Q, et al. A practical guide to treatment of infantile hemangiomas of the head and neck. Int J Clin Exp Med. 2013;6(10):851-60.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3832322/?report=classic#
  7. ↑ 7.0 7.1 7.2 7.3 Callahan, Alison B.; Yoon, Michael K. (2012). “Infantile hemangiomas: A review”. Saudi Journal of Ophthalmology. 26 (3): 283–291. doi:10.1016/j.sjopt.2012.05.004. ISSN 1319-4534.
  8. ↑ 8.0 8.1 Hemangioma. USPSTF. http://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=hemangioma Accessed on November 10, 2015
  9. ↑ 9.0 9.1 Hassan, Basheir A.; Shreef, Khalid S. (2014). “Propranolol in Treatment of Huge and Complicated Infantile Hemangiomas in Egyptian Children”. Dermatology Research and Practice. 2014: 1–5. doi:10.1155/2014/541810. ISSN 1687-6105.
  10. ↑ Ultrasound of Facial hemangioma. Dr Sinéad Culleton. Radiopaedia (2015). http://radiopaedia.org/cases/facial-haemangioma. Accessed on November 17, 2015

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nawal Muazam M.D.[2]

Overview

Hemangioma was first described by Dr. Robert Liston, a British surgeon, in 1843.[1]

Historical Perspective

Hemangioma was first described by Dr. Robert Liston, a British surgeon, in 1843.[1]

References

  1. ↑ 1.0 1.1 Liston R. Case of erectile tumour in the popliteal space.-Removal. Med Chir Trans. 1843;26:120-32.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2116921/pdf/medcht00056-0152.pdf

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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Nawal Muazam M.D.[2]

Overview

Hemangioma may be classified according to International Society for the Study of Vascular Anomalies into six subtypes: Infantile hemangioma, congenital hemangioma, tufted hemangioma, spindle-cell hemangioma, epithelioid hemangioma, and lobular capillary hemangioma.[1][2]

Classification

Hemangioma may be classified according to International Society for the Study of Vascular Anomalies into six subtypes:[1][2]

  • Infantile hemangioma
  • Congenital hemangioma
    • Rapidly involuting congenital hemangioma
    • Non-involuting congenital hemangioma
    • Partially involuting congenital hemangioma
  • Tufted angioma
  • Spindle-cell hemangioma
  • Epithelioid hemangioma
  • Lobular capillary hemangioma

References

  1. ↑ 1.0 1.1 Hemangioma. Dr Tim Luijkx and Dr Donna D’Souza et al. Radiopaedia (2015). http://radiopaedia.org/articles/haemangioma. Accessed on November 12, 2015
  2. ↑ 2.0 2.1 Richter, Gresham T.; Friedman, Adva B. (2012). “Hemangiomas and Vascular Malformations: Current Theory and Management”. International Journal of Pediatrics. 2012: 1–10. doi:10.1155/2012/645678. ISSN 1687-9740.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Nawal Muazam M.D.[2]

Overview

Development of hemangioma is the result of genetic mutations, overexpression of angiogenic fators and downregulation of inhibitors of angiogenesis. Hemangioma may be associated with POEMS syndrome and Castleman disease. On gross pathology, spongy with vascular compartments of various sizes separated by fibrous tissue are findings of hemangioma. On microscopic histopathological analysis, channels lined by benign endothelium containing red blood cells are findings of hemangioma.

Pathophysiology

The pathogenesis of hemangiomas has not been elucidated, but there are two competing theories;

First theory

Second theory

  • The second theory is that the presence of liver hemangiomas involves a genetic background of mutations.[1]
  • Genetic errors in growth factor receptors have also been shown to affect development of hemangiomas.
  • Metalloproteinases can accumulate in the endoplasmic reticulum of the tumor cells causing:
    • Self-digestion
    • Vacuole formation
  • Cavernous hemangioma cell can downregulate Derlin-1.
    • Derlin-1 is a protein that when overexpressed induces the dilated endoplasmic reticulum to return to its normal size.

Third theory

  • The third theory suggests that hemangioma endothelial cells arise from disrupted placental tissue imbedded in fetal soft tissues during gestation or birth.[2]
  • Markers of hemangiomas have been shown to coincide with those found in placental tissue.
  • This is further supported by the fact that they are found more commonly in infants following:[2]

Growth Pattern

  • Hemangiomas follow a predictable course with three distinct developmental phases:[2]
Proliferation phase
  • In most hemangiomas, eighty percent of proliferation occurs by three months of life but may last longer.[2][3]
  • During proliferation, rapid growth can lead to exhaustion of blood supply with resulting ischemia, necrosis, ulceration, and bleeding.
Quiescence phase
  • Following proliferation, hemangiomas enter a slower or no growth phase, known as quiescence.[2]
  • This phase typically lasts from nine to twelve months of age.
Involution phase
  • The final and unique phase of the hemangioma lifecycle is involution.[2]
  • This phase is marked by graying of the overlying skin and shrinking of the deeper components.
  • At the final stages of involution, a fibrofatty protuberance may remain.

Associated Conditions

Hemangioma may be associated with:

Gross Pathology

  • Grossly hemangiomas are described as “spongy” with vascular compartments of various sizes separated by fibrous tissue.[1]
  • Thrombi may be present and are well separated from the normal liver parenchyma despite the absence of a fibrous capsule.

Microscopic Pathology

On microscopic histopathological analysis channels lined by benign endothelium containing red blood cells are findings of hemangioma.[3]

  • Intermediate magnification micrograph of a capillary hemangioma. H&E stain.[3]
    Intermediate magnification micrograph of a capillary hemangioma. H&E stain.[3]
  • Very high magnification micrograph of a capillary hemangioma. H&E stain.[3]
    Very high magnification micrograph of a capillary hemangioma. H&E stain.[3]
  • Histopathological image representing a cavernous hemangioma of the liver. Surgical excision of the lesion for the impending risk for rupture. H&E stain.[3]
    Histopathological image representing a cavernous hemangioma of the liver. Surgical excision of the lesion for the impending risk for rupture. H&E stain.[3]
  • Histopathological image reprsenting a cavernous hemangioma of the liver. H&E stain.[3]
    Histopathological image reprsenting a cavernous hemangioma of the liver. H&E stain.[3]

Immunohistochemistry

Hemangioma is demonstrated by positivity to:[3]

  • CD31 positive
  • D2-40 negative

References

  1. ↑ 1.0 1.1 1.2 1.3 Papafragkakis, Haris; Moehlen, Martin; Garcia-Buitrago, Monica T.; Madrazo, Beatrice; Island, Eddie; Martin, Paul (2011). “A Case of a Ruptured Sclerosing Liver Hemangioma”. International Journal of Hepatology. 2011: 1–5. doi:10.4061/2011/942360. ISSN 2090-3456.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Richter, Gresham T.; Friedman, Adva B. (2012). “Hemangiomas and Vascular Malformations: Current Theory and Management”. International Journal of Pediatrics. 2012: 1–10. doi:10.1155/2012/645678. ISSN 1687-9740.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Microscopic features of hemangioma. Librepathology (2015). http://librepathology.org/wiki/index.php/Hemangioma. Accessed on November 12, 2015

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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nawal Muazam M.D.[2]

Overview

There are no established causes for hemangioma.[1][2]

Causes

There are no established causes for hemangioma.[1][2]

References

  1. ↑ 1.0 1.1 Zheng JW, Zhang L, Zhou Q, et al. A practical guide to treatment of infantile hemangiomas of the head and neck. Int J Clin Exp Med. 2013;6(10):851-60.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3832322/?report=classic#
  2. ↑ 2.0 2.1 Jr, Marcelo AF Ribeiro (2010). “Spontaneous rupture of hepatic hemangiomas: A review of the literature”. World Journal of Hepatology. 2 (12): 428. doi:10.4254/wjh.v2.i12.428. ISSN 1948-5182.

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Differentiating Hemangioma from other Diseases

Differentiating Hemangioma from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Nawal Muazam M.D.[2]

Overview

Hemangioma must be differentiated from other diseases such as: congenital hemangioma, kaposiform hemangioendothelioma, tufted angioma, nevus flammeus, and pyogenic granuloma.[1]

Hemangioma differential diagnosis

Hemangioma must be differentiated from other diseases such as:[1]

Differential Diagnosis of Cardiac Hemangioma

Cardiac hemangioma should be differentiated from other cardiac tumors that present as a cardiac mass. The following are the differentials:[2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48]

Site of Tumor Malignant Potential Type of Tumor Tissue of Origin Age of Presentation Location Morphology Signs and Symptoms MRI Findings
Systemic Manifestations Cardiac Manifestations Embolic Manifestations
Primary Cardiac Tumor Primary Benign Myxoma
  • Between third to sixth decade of life
  • 1-15 cm in diameter
  • Pedunculated
  • Polypoid
  • Smooth and lobulated
  • Villous and pappillary appearance associated with embolization
Rhabdomyoma
  • Striated Muscle
  • 1-3 cm in size
  • Yellow-gray color
  • Firm
  • Circumscribed lobulated
  • Majority multiple if associated with tuberous sclerosis (of those with no association, 50% are single)
  • Multiple masses isointense to muscle tissue on T1 images
  • Hyperintense on T2 images
Cardiac Fibroma
  • Children (1/3rd in infants)
  • Solitary
  • Solitary mass
  • Low intensity on T2 weighted image
Fibroelastoma
  • < 1 cm in diameter
  • Solitary
  • Papillary
  • Flower-like appearance with multiple attachments to valve
  • Short pedicle
  • T1 and T2 weighted images show uniform intermediate signal intensity similar to myocardium
  • Homogeneous late gadolinium contrast enhancement
Hemangioma
  • < 1 year to 70 years
  • < 2 % of primary cardiac tumors
  • Polypoid
  • Encapsulated
  • Intermediate density on T1 images
  • Hypointense on T2 images
  • Multicystic enhancing lesion
  • Involvement of epicardium or pericardium
Lipoma
  • Between fourth to sixth decade of life
  • Epicardial or intramural lesion
  • High intensity on T1 weighted image
  • Drop out on fat saturation images
Paraganglioma
  • Average age of presentation is 11-13 years
    • 3-8 cm
    • Well-defined
    • Broad base
    • Encapsulated
    • Heterogeneous
    • Hypervascular
    Atrioventricular Node Tumor
    • Average age of diagnosis is 38 years
    • Female to male ratio 3:1
    • Hypointense cardiac mass on standard imaging
    • Hyperintensity on late gadolinium enhancement (LGE) images with heterogeneous contrast enhancement
    Lipomatous hypertrophy of the interatrial septum
    • > 60 years
    		 –
    Primary Malignant Fibrosarcoma
    • 20 to 80 years
    • Sessile or pedunculated protruding masses in ventricular cavities
    • Soft
    • Lobulated
    • Gelatinous
    • Heterogenous or isointense to myocardium on T1 weighted images
    Angiosarcoma
    • 30 to 50 years
    • Arterial phase enhancement
    Rhabdomyosarcoma
    • Most common primary sarcoma of children
    • Average age of presentation is 20 years
    • Multiple
    • Three types:
      • Embryonic
      • Pleomorphic
      • Alveolar
    • Intermediate-to-hypointensity compared with muscle on T1 images
    • Hyperintense on T2-weighted imaging with heterogeneous contrast enhancement
    Lymphoma
    • 10 to 90 years
    • Males > females
    • Right sided mostly
    • Majority solitary (1/3rd multiple)
    • Hypointense on T1-weighted images and hyperintense on T2-weighted images
    Secondary Cardiac Tumor Metastastatic Malignant Metastasis
    • Any age
    • Multiple

      References

      1. ↑ 1.0 1.1 Callahan, Alison B.; Yoon, Michael K. (2012). “Infantile hemangiomas: A review”. Saudi Journal of Ophthalmology. 26 (3): 283–291. doi:10.1016/j.sjopt.2012.05.004. ISSN 1319-4534.
      2. ↑ Mankad R, Herrmann J (December 2016). “Cardiac tumors: echo assessment”. Echo Res Pract. 3 (4): R65–R77. doi:10.1530/ERP-16-0035. PMC 5292983. PMID 27600455.
      3. ↑ Zaragoza-Macias E, Zaragosa-Macias E, Chen MA, Gill EA (February 2012). “Real time three-dimensional echocardiography evaluation of intracardiac masses”. Echocardiography. 29 (2): 207–19. doi:10.1111/j.1540-8175.2011.01627.x. PMID 22283202.
      4. ↑ Larrieu AJ, Jamieson WR, Tyers GF, Burr LH, Munro AI, Miyagishima RT, Gerein AN, Allen P (March 1982). “Primary cardiac tumors: experience with 25 cases”. J. Thorac. Cardiovasc. Surg. 83 (3): 339–48. PMID 7062746.
      5. ↑ Molina JE, Edwards JE, Ward HB (August 1990). “Primary cardiac tumors: experience at the University of Minnesota”. Thorac Cardiovasc Surg. 38 Suppl 2: 183–91. doi:10.1055/s-2007-1014064. PMID 2237900.
      6. ↑ Tazelaar HD, Locke TJ, McGregor CG (October 1992). “Pathology of surgically excised primary cardiac tumors”. Mayo Clin. Proc. 67 (10): 957–65. PMID 1434856.
      7. ↑ Sarjeant JM, Butany J, Cusimano RJ (2003). “Cancer of the heart: epidemiology and management of primary tumors and metastases”. Am J Cardiovasc Drugs. 3 (6): 407–21. doi:10.2165/00129784-200303060-00004. PMID 14728061.
      8. ↑ St John Sutton MG, Mercier LA, Giuliani ER, Lie JT (June 1980). “Atrial myxomas: a review of clinical experience in 40 patients”. Mayo Clin. Proc. 55 (6): 371–6. PMID 7382545.
      9. ↑ Pinede L, Duhaut P, Loire R (May 2001). “Clinical presentation of left atrial cardiac myxoma. A series of 112 consecutive cases”. Medicine (Baltimore). 80 (3): 159–72. PMID 11388092.
      10. ↑ Reynen K (December 1995). “Cardiac myxomas”. N. Engl. J. Med. 333 (24): 1610–7. doi:10.1056/NEJM199512143332407. PMID 7477198.
      11. ↑ Javed A, Zalawadiya S, Kovach J, Afonso L (March 2014). “Aortic valve myxoma at the extreme age: a review of literature”. BMJ Case Rep. 2014. doi:10.1136/bcr-2013-202689. PMC 3962858. PMID 24642215.
      12. ↑ Lee VH, Connolly HM, Brown RD (August 2007). “Central nervous system manifestations of cardiac myxoma”. Arch. Neurol. 64 (8): 1115–20. doi:10.1001/archneur.64.8.1115. PMID 17698701.
      13. ↑ Carney JA, Gordon H, Carpenter PC, Shenoy BV, Go VL (July 1985). “The complex of myxomas, spotty pigmentation, and endocrine overactivity”. Medicine (Baltimore). 64 (4): 270–83. PMID 4010501.
      14. ↑ McAllister HA, Hall RJ, Cooley DA (February 1999). “Tumors of the heart and pericardium”. Curr Probl Cardiol. 24 (2): 57–116. PMID 10028128.
      15. ↑ Klarich KW, Enriquez-Sarano M, Gura GM, Edwards WD, Tajik AJ, Seward JB (September 1997). “Papillary fibroelastoma: echocardiographic characteristics for diagnosis and pathologic correlation”. J. Am. Coll. Cardiol. 30 (3): 784–90. PMID 9283541.
      16. ↑ Tamin SS, Maleszewski JJ, Scott CG, Khan SK, Edwards WD, Bruce CJ, Oh JK, Pellikka PA, Klarich KW (June 2015). “Prognostic and Bioepidemiologic Implications of Papillary Fibroelastomas”. J. Am. Coll. Cardiol. 65 (22): 2420–9. doi:10.1016/j.jacc.2015.03.569. PMID 26046736.
      17. ↑ Gowda RM, Khan IA, Nair CK, Mehta NJ, Vasavada BC, Sacchi TJ (September 2003). “Cardiac papillary fibroelastoma: a comprehensive analysis of 725 cases”. Am. Heart J. 146 (3): 404–10. doi:10.1016/S0002-8703(03)00249-7. PMID 12947356.
      18. ↑ Beghetti M, Gow RM, Haney I, Mawson J, Williams WG, Freedom RM (December 1997). “Pediatric primary benign cardiac tumors: a 15-year review”. Am. Heart J. 134 (6): 1107–14. PMID 9424072.
      19. ↑ Smythe JF, Dyck JD, Smallhorn JF, Freedom RM (November 1990). “Natural history of cardiac rhabdomyoma in infancy and childhood”. Am. J. Cardiol. 66 (17): 1247–9. PMID 2239731.
      20. ↑ Jacobs JP, Konstantakos AK, Holland FW, Herskowitz K, Ferrer PL, Perryman RA (November 1994). “Surgical treatment for cardiac rhabdomyomas in children”. Ann. Thorac. Surg. 58 (5): 1552–5. PMID 7979700.
      21. ↑ Elbardissi AW, Dearani JA, Daly RC, Mullany CJ, Orszulak TA, Puga FJ, Schaff HV (September 2008). “Survival after resection of primary cardiac tumors: a 48-year experience”. Circulation. 118 (14 Suppl): S7–15. doi:10.1161/CIRCULATIONAHA.107.783126. PMID 18824772.
      22. ↑ Basu S, Folliguet T, Anselmo M, Greengart A, Sabado M, Cunningham JN, Jacobowitz IJ (April 1994). “Lipomatous hypertrophy of the interatrial septum”. Cardiovasc Surg. 2 (2): 229–31. PMID 8049952.
      23. ↑ Simpson L, Kumar SK, Okuno SH, Schaff HV, Porrata LF, Buckner JC, Moynihan TJ (June 2008). “Malignant primary cardiac tumors: review of a single institution experience”. Cancer. 112 (11): 2440–6. doi:10.1002/cncr.23459. PMID 18428209.
      24. ↑ Vander Salm TJ (April 2000). “Unusual primary tumors of the heart”. Semin. Thorac. Cardiovasc. Surg. 12 (2): 89–100. PMID 10807431.
      25. ↑ Petersen CD, Robinson WA, Kurnick JE (1976). “Involvement of the heart and pericardium in the malignant lymphomas”. Am. J. Med. Sci. 272 (2): 161–5. PMID 1008078.
      26. ↑ Ragland MM, Tak T (March 2006). “The role of echocardiography in diagnosing space-occupying lesions of the heart”. Clin Med Res. 4 (1): 22–32. PMC 1447535. PMID 16595790.
      27. ↑ Miguel CE, Bestetti RB (June 2011). “Primary cardiac lymphoma”. Int. J. Cardiol. 149 (3): 358–63. doi:10.1016/j.ijcard.2010.02.016. PMID 20227122.
      28. ↑ Grebenc ML, Rosado de Christenson ML, Burke AP, Green CE, Galvin JR (2000). “Primary cardiac and pericardial neoplasms: radiologic-pathologic correlation”. Radiographics. 20 (4): 1073–103, quiz 1110–1, 1112. doi:10.1148/radiographics.20.4.g00jl081073. PMID 10903697.
      29. ↑ Grinda JM, Couetil JP, Chauvaud S, D’Attellis N, Berrebi A, Fabiani JN, Deloche A, Carpentier A (January 1999). “Cardiac valve papillary fibroelastoma: surgical excision for revealed or potential embolization”. J. Thorac. Cardiovasc. Surg. 117 (1): 106–10. PMID 9869763.
      30. ↑ Webb DW, Thomas RD, Osborne JP (March 1993). “Cardiac rhabdomyomas and their association with tuberous sclerosis”. Arch. Dis. Child. 68 (3): 367–70. PMC 1793857. PMID 8466239.
      31. ↑ Yoshitake I, Hata M, Sezai A, Niino T, Unosawa S, Shimura K, Kasamaki Y, Minami K (September 2009). “Cardiac angiosarcoma with cardiac tamponade diagnosed as a ruptured aneurysm of the sinus valsalva”. Jpn. J. Clin. Oncol. 39 (9): 612–5. doi:10.1093/jjco/hyp044. PMID 19493870.
      32. ↑ Parissis H, Akbar MT, Young V (October 2010). “Primary leiomyosarcoma of the right atrium: a case report and literature update”. J Cardiothorac Surg. 5: 80. doi:10.1186/1749-8090-5-80. PMC 2964688. PMID 20939891.
      33. ↑ Gulati G, Sharma S, Kothari SS, Juneja R, Saxena A, Talwar KK (2004). “Comparison of echo and MRI in the imaging evaluation of intracardiac masses”. Cardiovasc Intervent Radiol. 27 (5): 459–69. doi:10.1007/s00270-004-0123-4. PMID 15383848.
      34. ↑ Narin B, Arman A, Arslan D, Simşek M, Narin A (February 2010). “Assessment of cardiac masses: magnetic resonance imaging versus transthoracic echocardiography”. Anadolu Kardiyol Derg. 10 (1): 69–74. PMID 20150010.
      35. ↑ “academic.oup.com”.
      36. ↑ Ismail I, Al-Khafaji K, Mutyala M, Aggarwal S, Cotter W, Hakim H, Khosla S, Arora R (2015). “Cardiac lipoma”. J Community Hosp Intern Med Perspect. 5 (5): 28449. doi:10.3402/jchimp.v5.28449. PMC 4612478. PMID 26486106.
      37. ↑ D’Souza J, Shah R, Abbass A, Burt JR, Goud A, Dahagam C (January 2017). “Invasive Cardiac Lipoma: a case report and review of literature”. BMC Cardiovasc Disord. 17 (1): 28. doi:10.1186/s12872-016-0465-2. PMC 5237479. PMID 28088193.
      38. ↑ Yadav, Pradeep K.; Baquero, Giselle A.; Malysz, Jozef; Kelleman, John; Gilchrist, Ian C. (2014). “Cardiac Paraganglioma”. Circulation: Cardiovascular Interventions. 7 (6): 851–856. doi:10.1161/CIRCINTERVENTIONS.114.001856. ISSN 1941-7640.
      39. ↑ Tahir M, Noor SJ, Herle A, Downing S (2009). “Right atrial paraganglioma: a rare primary cardiac neoplasm as a cause of chest pain”. Tex Heart Inst J. 36 (6): 594–7. PMC 2801953. PMID 20069088.
      40. ↑ Hamilton BH, Francis IR, Gross BH, Korobkin M, Shapiro B, Shulkin BL, Deeb CM, Orringer MB (January 1997). “Intrapericardial paragangliomas (pheochromocytomas): imaging features”. AJR Am J Roentgenol. 168 (1): 109–13. doi:10.2214/ajr.168.1.8976931. PMID 8976931.
      41. ↑ Shih, Wei-Jen; McCullough, Scott; Smith, Mary (1993). “Diagnostic imagings for primary cardiac fibrosarcoma”. International Journal of Cardiology. 39 (2): 157–161. doi:10.1016/0167-5273(93)90028-F. ISSN 0167-5273.
      42. ↑ Arai T, Kurashima C, Wada S, Chida K, Ohkawa S (November 1998). “Histological evidence for cell proliferation activity in cystic tumor (endodermal heterotopia) of the atrioventricular node”. Pathol. Int. 48 (11): 917–23. PMID 9832064.
      43. ↑ Wolf PL, Bing R (November 1965). “The smallest tumor which causes sudden death”. JAMA. 194 (6): 674–5. PMID 5897246.
      44. ↑ Burke AP, Anderson PG, Virmani R, James TN, Herrera GA, Ceballos R (October 1990). “Tumor of the atrioventricular nodal region. A clinical and immunohistochemical study”. Arch. Pathol. Lab. Med. 114 (10): 1057–62. PMID 2222148.
      45. ↑ Burke A, Tavora F (April 2016). “The 2015 WHO Classification of Tumors of the Heart and Pericardium”. J Thorac Oncol. 11 (4): 441–52. doi:10.1016/j.jtho.2015.11.009. PMID 26725181.
      46. ↑ Tran, Thao T; Starnes, Vaughn; Wang, Xuedong; Getzen, James; Ross, Brian D (2009). “Cardiovascular magnetics resonance diagnosis of cystic tumor of the atrioventricular node”. Journal of Cardiovascular Magnetic Resonance. 11 (1): 13. doi:10.1186/1532-429X-11-13. ISSN 1532-429X.
      47. ↑ Tatli, Servet; O’Gara, Patrick Thomas; Lambert, Jarvis; Kwong, Raymond; Byrne, John Gerald; Yucel, E. Kent (2004). “MRI of Atypical Lipomatous Hypertrophy of the Interatrial Septum”. American Journal of Roentgenology. 182 (3): 598–600. doi:10.2214/ajr.182.3.1820598. ISSN 0361-803X.
      48. ↑ Saboo, Sachin S.; Krajewski, Katherine M.; Zukotynski, Katherine; Howard, Stephanie; Jagannathan, Jyothi P.; Hornick, Jason L.; Ramaiya, Nikhil (2012). “Imaging Features of Primary and Secondary Adult Rhabdomyosarcoma”. American Journal of Roentgenology. 199 (6): W694–W703. doi:10.2214/AJR.11.8213. ISSN 0361-803X.

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      Epidemiology and Demographics

      Epidemiology and Demographics

      Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Nawal Muazam M.D.[2]

      Overview

      The prevalence of infantile hemangioma is estimated to be up to 10% in general population.[1] Hemangioma commonly affects infants.[2] Females are more commonly affected with hemangioma than males.[2][3]

      Epidemiology and demographics

      Prevalence

      Infantile hemangiomas are the most common tumor in infancy and occur in approximately 10,000 out of 100,000 infants.[1]

      Age

      Hemangioma commonly affects infants.[2]

      Gender

      Females are three to five times more likely to have hemangiomas than males.[2][3]

      Race

      Hemangiomas occur in approximately ten percent of caucasians, and are less prevalent in other races.[2][3]

      References

      1. ↑ 1.0 1.1 Richter, Gresham T.; Friedman, Adva B. (2012). “Hemangiomas and Vascular Malformations: Current Theory and Management”. International Journal of Pediatrics. 2012: 1–10. doi:10.1155/2012/645678. ISSN 1687-9740.
      2. ↑ 2.0 2.1 2.2 2.3 2.4 Zheng JW, Zhang L, Zhou Q, et al. A practical guide to treatment of infantile hemangiomas of the head and neck. Int J Clin Exp Med. 2013;6(10):851-60.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3832322/?report=classic#
      3. ↑ 3.0 3.1 3.2 Caucanas, Marie; Paquet, Philippe; Henry, Frédérique; Piérard-Franchimont, Claudine; Reginster, Marie-Annick; Piérard, Gérald E. (2011). “Intense Pulsed-Light Therapy for Proliferative Haemangiomas of Infancy”. Case Reports in Dermatological Medicine. 2011: 1–5. doi:10.1155/2011/253607. ISSN 2090-6463.

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      Risk Factors

      Risk Factors

      Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Nawal Muazam M.D.[2]

      Overview

      Common risk factors in the development of hemangioma are female gender, prematurity, low birth weight, and fair skin.

      Risk Factors

      Common risk factors in the development of hemangioma are:[1]

      References

      1. ↑ Richter, Gresham T.; Friedman, Adva B. (2012). “Hemangiomas and Vascular Malformations: Current Theory and Management”. International Journal of Pediatrics. 2012: 1–10. doi:10.1155/2012/645678. ISSN 1687-9740.

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      Screening

      Screening

      Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nawal Muazam M.D.[2]

      Overview

      According to the United States Preventive Services Task Force, there is insufficient evidence to recommend routine screening for hemangioma.[1]

      Hemangioma screening

      According to the United States Preventive Services Task Force, there is insufficient evidence to recommend routine screening for hemangioma.[1]

      References

      1. ↑ 1.0 1.1 Hemangioma. USPSTF. http://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=hemangioma Accessed on November 10, 2015

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      Natural History, Complications and Prognosis

      Natural History, Complications and Prognosis

      Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Nawal Muazam M.D.[2]

      Overview

      If left untreated, 20% of patients with hemangioma may progress to develop ulceration, hemorrhage, infection, and high output cardiac failure. Common complications of hemangioma include ischemia, necrosis, ulceration, and bleeding. Prognosis is generally good.

      Natural history

      Hemangiomas are vascular tumors that are rarely apparent at birth, grow rapidly during the first six months of life, involute with time and do not necessarily infiltrate but can sometimes be destructive.[1][2]

      Complications

      Rapid growth of hemangiomas can lead to exhaustion of blood supply with resulting:[1]

      Ophthalmic complications

      Common complications of infantile hemangioma include:[3]

      Prognosis

      Hemangioma generally has a good prognosis and is cosidered as a benign condition.

      References

      1. ↑ 1.0 1.1 Richter, Gresham T.; Friedman, Adva B. (2012). “Hemangiomas and Vascular Malformations: Current Theory and Management”. International Journal of Pediatrics. 2012: 1–10. doi:10.1155/2012/645678. ISSN 1687-9740.
      2. ↑ Hassan, Basheir A.; Shreef, Khalid S. (2014). “Propranolol in Treatment of Huge and Complicated Infantile Hemangiomas in Egyptian Children”. Dermatology Research and Practice. 2014: 1–5. doi:10.1155/2014/541810. ISSN 1687-6105.
      3. ↑ Callahan, Alison B.; Yoon, Michael K. (2012). “Infantile hemangiomas: A review”. Saudi Journal of Ophthalmology. 26 (3): 283–291. doi:10.1016/j.sjopt.2012.05.004. ISSN 1319-4534.

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      Diagnosis

      Diagnosis

      Diagnostic Study of Choice | Staging | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X Ray | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

      Treatment

      Treatment

      Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

      Case Studies

      Case Studies

      Case #1

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